Evidence map›Paper›PMID 10811875›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

Ski acts as a co-repressor with Smad2 and Smad3 to regulate the response to type beta transforming growth factor.

W Xu, K Angelis, D Danielpour, M M Haddad, O Bischof, J Campisi, E Stavnezer, E E Medrano

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
5.4field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 191 citations in OpenAlex.

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  12. Article
  13. TGFB1/INHBA Homodimer/Nodal-SMAD2/3 Signaling Network: A Pivotal Molecular Target in PDAC Treatment.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Blood · 2018
    Article
  19. Article
  20. Article

6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

W XuHuffington Center on Aging and Departments of Molecular and Cellular Biology and Dermatology, Baylor College of Medicine and Veterans Affairs Medical Center, Houston, TX 77030, USA.
K Angelis
D Danielpour
M M Haddad
O Bischof
J Campisi
E Stavnezer
E E Medrano
Baylor College of Medicine · USCase Western Reserve University · USLawrence Berkeley National Laboratory · US

Funding

TUMOR METABOLISM PROGRAMP30CA043703 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI MARK R CHANCE · 1987 to 2026
$142.3M
ORIGIN, STRUCTURE, AND BIOLOGICAL ACTIVITY OF SKVSR01CA043600 · NCI · UNIVERSITY OF CINCINNATI · PI STAVNEZER, EDWARD · 1986 to 2003
$1.2M
NCI NIH HHS CA-43600NCI NIH HHS P30 CA043703NCI NIH HHS R01 CA043600NIA NIH HHS AG-09990NIA NIH HHS AG-3663
6 · The paper itself

Abstract

The c-ski protooncogene encodes a transcription factor that binds DNA only in association with other proteins. To identify co-binding proteins, we performed a yeast two-hybrid screen. The results of the screen and subsequent co-immunoprecipitation studies identified Smad2 and Smad3, two transcriptional activators that mediate the type beta transforming growth factor (TGF-beta) response, as Ski-interacting proteins. In Ski-transformed cells, all of the Ski protein was found in Smad3-containing complexes that accumulated in the nucleus in the absence of added TGF-beta. DNA binding assays showed that Ski, Smad2, Smad3, and Smad4 form a complex with the Smad/Ski binding element GTCTAGAC (SBE). Ski repressed TGF-beta-induced expression of 3TP-Lux, the natural plasminogen activator inhibitor 1 promoter and of reporter genes driven by the SBE and the related CAGA element. In addition, Ski repressed a TGF-beta-inducible promoter containing AP-1 (TRE) elements activated by a combination of Smads, Fos, and/or Jun proteins. Ski also repressed synergistic activation of promoters by combinations of Smad proteins but failed to repress in the absence of Smad4. Thus, Ski acts in opposition to TGF-beta-induced transcriptional activation by functioning as a Smad-dependent co-repressor. The biological relevance of this transcriptional repression was established by showing that overexpression of Ski abolished TGF-beta-mediated growth inhibition in a prostate-derived epithelial cell line.

Indexed as

Cell NucleusDNA-Binding ProteinsFemaleGene Expression RegulationGene Expression Regulation, NeoplasticGenes, ReporterHumansLuciferasesMacromolecular SubstancesMelanomaNeoplasm ProteinsPromoter Regions, GeneticProto-Oncogene ProteinsRecombinant Fusion ProteinsRepressor ProteinsSmad2 ProteinDNA-Binding ProteinsLuciferasesMacromolecular SubstancesNeoplasm ProteinsProto-Oncogene ProteinsRecombinant Fusion ProteinsRepressor ProteinsSKI protein, humanSmad2 ProteinSMAD2 protein, humanSmad3 ProteinSMAD3 protein, humanTrans-ActivatorsTranscription FactorsTransforming Growth Factor beta

Identifiers

PMID10811875
PMCPMC18535
OpenAlexW2009609922

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.